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Annals of Oncology (12.1%) discontinued NPLD treatment due to toxicity. In those, 9 (6.4%) patients experienced cardiac toxicity (grade 2 or 3) . There were 2 (1.4%) deaths related to cardiac toxicity. Conclusion: Re-challenge by an anthracycline-containing regimen should been considered in patients with MBC taking into account this encouraging ORR and the length of PFS and response duration. However cardiac safety of patients must be carefully investigated during the treatment taking into account the number of treatment cessation due to cardiac damage. Of interest the subset of patients with HER2 positive tumour seemed to highly benefit from the NLPD. This finding emphasizes the sensitivity to anthracycline in this subset of HER2 positive tumours and oncologist should not forgot anthracycline containing regimen as a possible option in MBC after failure to numerous lines including chemotherapy and HER2 targeted agents. Disclosure: All authors have declared no conflicts of interest. 358P PHARMACOKINETICS OF ERIBULIN MESILATE IN COMBINATION WITH CAPECITABINE IN PATIENTS WITH ADVANCED/METASTATIC CANCER: RESULTS FROM A PHASE IB DOSE-ESCALATION STUDY C.J. Twelves 1 , M. Nasim 2 , A. Anthoney 1 ,N.Cresti 3 , C. Savulsky 4 , C. Johnston 4 , L. Reyderman 5 , J. Wanders 4 , R. Plummer 3 , T.R.J. Evans 2 1 Clinical Cancer Research Groups, Leeds Institute of Molecular Medicine and St James’s Institute of Oncology, Leeds, UNITED KINGDOM, 2 Medical Oncology, Beatson West of Scotland Cancer Centre, Glasgow, UNITED KINGDOM, 3 Medical Oncology, Northern Institute for Cancer Research, University of Newcastle upon Tyne, Newcastle, UNITED KINGDOM, 4 Medical Oncology, Eisai Ltd, Hatfield, UNITED KINGDOM, 5 Medical Oncology, Eisai Inc., Woodcliff Lake, NJ, UNITED STATES OF AMERICA Background: Eribulin is a microtubule dynamics inhibitor EMA approved for certain patients (pts) with locally advanced (LA)/metastatic breast cancer (MBC) who have received ≥2 prior chemotherapeutic regimens for advanced disease. Prior therapy should have included an anthracycline and taxane. This Phase Ib, open-label dose-escalation study assessed maximum tolerated dose (MTD), safety and pharmacokinetics (PK) of eribulin in combination with capecitabine in pts with advanced/metastatic cancer. Methods: Pts received eribulin mesilate (2–5-min IV) by Schedule 1 (1.2, 1.6 or 2.0 mg/m 2 on Day [D] 1) or Schedule 2 (0.7, 1.1 or 1.4 mg/m 2 on D1 and D8) in combination with twice-daily oral capecitabine 1000 mg/m 2 on D1–14 every 21 days. To assess PK and drug-drug interaction of eribulin, capecitabine and capecitabine metabolites in Cycle 1 and 2, samples were taken on D1 (pre-, 0, 0.25, 0.5, 1–4, 6 and 8 h post-dose), any time on D2–3 and D4–6, and D8 (Schedule 1: pre-, 0.5, 1–4 and 6 h post-capecitabine; Schedule 2: pre-dose). PK was examined by non-compartmental analysis, and cardiac repolarization by 12-lead ECGs at screening, D1 (pre- and 4 h post-dose), D2–3, D8 and D15. Correlation of eribulin and capecitabine plasma concentrations with change from baseline (Δ) QTc was explored. Results: Schedule 1 (n = 19) and Schedule 2 (n = 15) MTDs were 1.6 and 1.4 mg/ m 2 eribulin mesilate, respectively. Dose-limiting toxicities (all n = 1) were: Grade (G) 4 neutropenia, G3 febrile neutropenia, G3 fatigue, G3 lethargy (Schedule 1); G4 neutropenic sepsis, G3 neutropenia (Schedule 2). There were no unexpected toxicities. Eribulin PK was independent of schedule and had dose-related increases in exposure. No accumulation occurred upon multiple dosing; at each dose, eribulin PK was comparable in Cycles 1 and 2. Exposure to capecitabine and metabolites was variable and independent of schedule. Co-administration had no effect on ΔQTc. Conclusions: No drug-drug interaction of eribulin and capecitabine was observed. From these results, the combination appears to be tolerated without effect on cardiac repolarization. A Phase II LA/MBC study evaluating Schedule 2 MTD is ongoing. Disclosure: C.J. Twelves: The author declares the following conflicts of interest: consultant/advisory role (Eisai) and honoraria/speakers bureau (Eisai). C. Savulsky: The author declares the following conflicts of interest: employee (Eisai Ltd). C. Johnston: The author declares the following conflicts of interest: employee (Eisai Ltd). L. Reyderman: The author declares the following conflicts of interest: employee (Eisai Inc.). J. Wanders: The author declares the following conflicts of interest: employee at the time of study (Eisai Ltd). R. Plummer: The author declares the following conflicts of interest: research funding (Eisai Ltd). T.R..J. Evans: The author declares the following conflicts of interest: research funding (Eisai Ltd). All other authors have declared no conflicts of interest. 359P ACTIVITY AND SAFETY OF A COMBINATION OF EPIRUBICIN, DOCETAXEL AND CISPLATIN AS NEOADJUVANT TREATMENT FOR LOCALLY ADVANCED BREAST CANCER (LABC): A PRELIMINARY REPORT N. Avci 1 , O. Kanat 1 , S. Gokgoz 2 , S. Tolunay 3 , U. Topal 4 , E. Cubukcu 1 , F. Olmez 1 1 Medical Oncology, Uludag University Faculty of Medicine, Bursa, TURKEY, 2 Surgery, Uludag University Faculty of Medicine, Bursa, TURKEY, 3 Pathology, Uludag University Faculty of Medicine, Bursa, TURKEY, 4 Radiology, Uludag University Faculty of Medicine, Bursa, TURKEY Aim and background: Efficacy of cisplatin-containing triplet chemotherapy regimens for neoadjuvant therapy of LABC has not been investigated extensively. The aim of this study was to evaluate activity and safety of a combination of epirubicin, docetaxel and cisplatin (ETC) in the neoadjuvant setting. Patients and methods: Forty-two patients with LABC (T2-T4, N0-N2, M0) were enrolled the study from March 2010 to April 2011. These patients received epirubicin (60 mg/m2 intravenously [I.V.] day 1), docetaxel (60 mg/m2 I.V. day 1) and cisplatin (60 mg/m2 I.V. day 1) every 21 days for at least 4 cycles, plus a final 2 additional cycles. Upon completion of therapy, the primary tumor was resected when not contraindicated. The primary endpoint was the pathological complete response (pCR) rate; seconday endpoints included response rate and toxicity. Results: Median patients age was 48 years (range, 23-73 years). Median tumor size was 3.2 cm. Thirty-seven patients (88%) received 6 cycles of ETC. The overall clinical response rate was 78.6%. Twenty of 42 patients (47.6%) achieved a complete pathological response (CPR). All tumors became operable after neoadjuvant chemotherapy. The most common side effect was myelotoxicity. WHO grade 4 neutropenia developed in 30 (73%) patients. No recurrence was observed in any patient after a mean follow-up of 17 months (13-21 months). Conclusion: Although our study group was small and the follow-up period relatively short-term, the considerably high rates of CPR in this preliminary series suggest that ETC regimen may be a promising option in neoadjuvant treatment of LABC. > Disclosure: All authors have declared no conflicts of interest. 360P SEQUENTIAL DOCETAXEL AS ADJUVANT CHEMOTHERAPY FOR NODE-POSITIVE OR/AND T3 OR T4 BREAST CANCER: CLINICAL OUTCOME (MANSOURA UNIVERSITY) H. Sakr 1 , R.H. Hamed 1 , A.H. Anter 1 , T. Yossef 2 1 Clinical Oncology and Nuclear Medicine, Mansoura University, Egypt, Mansoura, EGYPT, 2 General Surgery, Faculty of Medicine, Mansoura University, Mansoura, EGYPT Purpose: This trial compared six cycles of fluorouracil, epirubicin, and cyclophosphamide (FEC) with a sequential regimen of three cycles of FEC followed by three cycles of docetaxel (FEC-D) as adjuvant treatment for women with node-positive or/and T3 or T4 breast cancer. Patients and methods: Between January 2006 and January 2010, 657 patients with operable breast cancer were randomly assigned to either FEC every 21 days for six cycles, or three cycles of FEC followed by three cycles of docetaxel, both given every 21 days. Radiotherapy was mandatory for all patients who had undergone breast conserving surgery. Radiation to the chest wall, supraclavicular area, was recommended following mastectomy. Hormone-receptor–positive patients received tamoxifen for 5 years after chemotherapy. The primary end point was 5-year disease-free survival (DFS). Results: Median follow-up was 61 months. Five-year DFS rates were 74% with FEC and 78% with FEC-D (P= .013). Multivariate analysis adjusted for prognostic factors showed a 17% reduction in the relative risk of relapse with FEC-D. Five-year overall survival rates were 85% with FEC and 89.4% with FEC-D, demonstrating a 27% reduction in the relative risk of death (P= .014). The incidence of grade 3 to 4 neutropenia, the need for hematopoietic growth factor and incidence of nausea /vomiting were higher with FEC. Docetaxel was associated with more febrile neutropenia, stomatitis, edema, and nail disorders. Though rare overall, there were fewer cardiac events after FEC-D, attributable mainly to the lower anthracycline cumulative dose. Conclusion: Sequential adjuvant chemotherapy with FEC followed by docetaxel significantly improves disease free and overall survival in node-positive or/and T3 or T4 breast cancer patients and. Although the magnitude of the benefit observed with FEC-D, differences in the toxicity profiles of FEC and FEC-D may influence the choice of treatment for patients Disclosure: All authors have declared no conflicts of interest. Volume 23 | Supplement 9 | September 2012 doi:10.1093/annonc/mds393 | ix129
361P A RETROSPECTIVE ANALYSIS OF PLATINUM-BASED NEOADJUVANT CHEMOTHERAPY FOR LOCAL ADVANCED TRIPLE NEGATIVE BREAST CANCER F. Fei, Y. Du, X. Gu, C. Chen, J. Wu, Z. Shao Breast Surgery, Shanghai Cancer Center Fudan University, Shanghai, CHINA Purpose: We retrospectively analyzed platinum-based neoadjuvant chemotherapy for LATNBC to compare survival outcomes between patients with PCR and with non-PCR. Furthermore, the disease free survival of LATNBC patients with PCR continuously receiving primary regimen as adjuvant setting had comparative advantage concerning that of “PCR” patients switching to other regimens as adjuvant setting as well as those without any chemotherapy after sugery. Patients and methods: 124 women with stage II or III TNBCs experienced platinum-based regimens as neoadjuvant chemotherapy from Nov 1, 2007 to Dec 31, 2011. All patients were divided into the two groups, who were with and without PCR in the pathological reports after surgery. According to the adjuvant settings for LATNBC patients with PCR, the three arms were determined as continuous primary regimen (the same as neoadjuvant) arm, no more chemotherapy arm and switching arm. Disease free survival was computed using the Kaplan-Meier product limit method. Result: We presented a retrospective chart review of 124 LATNBC patients who underwent platinum-based neoadjuvant chemotherapy in our hospital. Fifty (40.32%) of those patients receiving neoadjuvant chemotherapy had PCR when they underwent surgery. After controlling for covariates associated with survival, patients undergoing neoadjuvant chemotherapy with residual tumor had significantly worse survival than patients with PCR (HR = 0.37,P < 0.05). Of 50 patients with PCR confirmed by surgery, the disease free survival of 24 cases switching to other regimens in the adjuvant setting was significantly better than that of 24 cases continuously receving primary regimens in the adjuvant setting (HR= 0.51, P = 0.025)and that of 2 cases with no more chemotherapy(HR= 0.58, P = 0.017) Conclusion: Patients with PCR had statistically significantly better clinical survival than those with non-PCR after platinum-based neoadjuvant settings.So far, if LATNBC patients with PCR after platinum-based neoadjuvant chemotherapy, they might have better clinical survival if they receive switching regimens than to receive primary regimens and to continue with no additional chemotherapy after surgery. A randomized prospective study needs to be carried out to strengthen the results because of statistical bias. Disclosure: All authors have declared no conflicts of interest. 362P MIGHT EARLY METABOLIC RESPONSE BY 18F-FDG-PET/CT BE USEFUL TO SELECT PATIENTS (PTS) WITH BREAST CANCER (BC) WHO WILL NOT OPTIMALLY RESPOND TO PREOPERATIVE CHEMOTHERAPY (PCT)? G. Zucchini1 , S. Quercia1 , C. Zamagni1 , D. Santini2 , M. Taffurelli3 , S. Fanti4 ,A. A. Martoni1 1 Medical Oncology Unit, S. Orsola-Malpighi University Hospital, Bologna, ITALY, 2 3 Pathology Unit, S. Orsola-Malpighi University Hospital, Bologna, ITALY, Breast Surgery Unit, S. Orsola-Malpighi University Hospital, Bologna, ITALY, 4 Department of Nuclear Medicine, S. Orsola-Malpighi University Hospital, Bologna, ITALY Purpose: To evaluate 18F-2-fluoro-2-deoxy-D-glucose positron emission tomography/computed tomography (18F-FDG PET/CT) changes between baseline and after 2 cycles of PCT in pts with early/locally advanced (E/LA) BC, with the aim to verify whether early metabolic assessment of response during PCT may have a role in clinical practice to enable early changes in the therapeutic strategy. Patients and methods: Sixty pts with newly diagnosed E/LA BC received 6-8 cycles of anthracycline and taxane-based PCT. Fifty-eight pts underwent surgery, which consisted in breast conserving surgery or radical mastectomy; axillary node dissection was performed in all cases. Optimal pathologic response (pR) to PCT was defined as absence of cancer cells in breast and ipsilateral axillary lymph nodes. All other conditions were defined as nonresponders (pNR). Maximum standardized uptake value (SUV max) with 18F-FDG PET/CT was measured for each pathologic lesion at baseline and after 2 cycles of PCT. SUV max percentage changes (Δ-SUV) were compared with pR rate according to immunohistochemical (IHC) BC characteristics. Δ-SUV >50% defined a metabolic response (MetR). Results: Thirteen (22%) of 60 pts achieved pR. According to IHC, pR rates where 16% in ERpositive/HER2negative (ER + /HER2-) pts, 29% and 27% in HER2-positive (HER2+) and triple negative (TN) pts respectively. Sensitivity of metR to identify pR was 100% in all three subgroups, but the specificity was low: 38% in ER + /HER2- pts (38%) was the highest value. In this subgroup of pts PET had a low positive predictive value (24%), while the negative predictive value was 100%, showing, compared to HER2+ and TN pts, the highest ability to correctly predict pNR (32%). At a median follow-up of 36.6 months, recurrence rate was higher in metabolic non-responders, particularly in the ER + /HER2- subgroup, in which Kaplan-Meier analysis of disease-free survival confirmed a significant difference (p = 0.0490). Conclusions: PET assay after 2 cycles of PCT correctly predicted pNR in 32% of ER + /HER2- pts, identifying a subgroup of BC pts with worse prognosis who might benefit from an early change of the therapeutic strategy. Disclosure: All authors have declared no conflicts of interest. 363P BREAST CANCER RECURRENCES AT THE CHEST WALL (BCRCW) WHEN STANDARD TREATMENTS (TX) HAVE FAILED: LYSO-THERMOSENSITIVE LIPOSOMAL DOXORUBICIN (LTLD) + MILD LOCAL HYPERTHERMIA (MLH) H.S. Rugo 1 , S.C. Formenti 2 , R.J. Myerson 3 , C.J. Diederich 4 , B.M. O’Connor 5 , A.J. Matzkowitz 6 , F. Muggia 7 1 Department of Medicine, University of California, San Francisco, CA, UNITED STATES OF AMERICA, 2 Radiation Oncology, NYU Langone Medical Center, NY, UNITED STATES OF AMERICA, 3 Radiation Oncology, Washington University School of Medicine in St. Louis, MO, UNITED STATES OF AMERICA, 4 Radiation Oncology, University of California, San Francisco, CA, UNITED STATES OF AMERICA, 5 Radiation Oncology, Commonwealth Atrius Cancer Center, MA, UNITED STATES OF AMERICA, 6 Radiation Oncology, Florida Cancer Specialists, New Port Richey, FL, UNITED STATES OF AMERICA, 7 Cancer Institute, NYU Langone Medical Center, New York, NY, UNITED STATES OF AMERICA Background: BCRCW has a poor prognosis, with disfigurement, pain, and restriction of movement. Study treatment consisted of LTLD that releases high concentrations of doxorubicin (Dox) in areas treated with mild hyperthermia at > 39.5°C. MLH kills tumor cells, selectively increases liposomal permeability in tumor microvasculature, releases Dox from LTLD, and promotes Dox tumor uptake. Methods: We conducted a phase I study of LTLD + MLH in patients (pts) with BCRCW tumors < 3 cm deep who had failed all standard Tx including surgery, radiation, and chemotherapy (CTx). Pts received up to 6 LTLD/MLH Txs every 21 days. Dosing cohorts started at 40 mg/m 2 and stopped escalation at 50 mg/m 2 . LTLD was infused IV over 30 minutes (min); then MLH was given by microwave or ultrasound. The thermal dose goal was 40°C-42°C for 60 min. Pharmacokinetic samples for total plasma Dox and doxorubicinol (Doxol) were taken at 0.5, 5, 10 and 24 hours after starting infusion. Results: Eleven pts with a median of 4 prior CTx (range 2 – 12) were enrolled; 10 had recurred after prior anthracycline (AC). All pts received > 2 cycles. The within subject variability in Dox and Doxol exposure was small with mean Cycle 2 vs Cycle 1 ratios ranging from 0.99 to 1.06. Cmax/dose (ng/ml)/(mg/m 2 Dox ) Doxol AUClast/dose ((ng*hr/ml)/(mg/m 2 ) Dox Doxol Annals of Oncology Cycle 1 499.82 0.46 1,338.18 7.96 Cycle 2 512.00 0.45 1,381.82 8.04 Two types of grade 3/4 toxicity were seen in > 5% of 42 cycles given: reversible neutropenia in 17 (40.5%) and reversible leukopenia in 9 (21.4%). One case (each) of mucositis (grade 1), chest wall thermal burn, and chest wall cellulitis (both grade 4) occurred, and no cases of cardiomyopathy or hand-foot toxicity were seen. The rate of clinically significant (> 6 point) QoL improvement on the FACT-B after 2 cycles was 54.5% (95% CI: 25.1% - 83.9%), including 1 lasting > 3 months. The local objective response rate was 45.5% (95% CI: 16.1% - 74.9%), with 1 complete and 4 partial local responses. Conclusion: LTLD + MLH is safe and active in BCRCW pts with prior radiation and AC exposure. A phase II study is underway. Disclosure: All authors have declared no conflicts of interest. 364P IMMUNOHISTOCHEMICAL PREDICTORS OF THE CLINICAL AND PATHOLOGICAL RESPONSE TO NEOADJUVANT CHEMOTHERAPY IN LOCALLY ADVANCED BREAST CANCER M. Rodionova 1 , D. Ryabchikov 1 , S. Portnoy 2 , I. Vorotnikov 1 , N. Chkhikvadze 1 1 Breast Cancer Department, N.N. Blokhin Russian Cancer Research Center, Moscow, RUSSIAN FEDERATION, 2 Department of Female Reproductive System Carcinomas, N.N.Blohkin Cancer Research Center, Moscow, RUSSIAN FEDERATION Purpose: To determine predictive immunohistochemical characteristics of the tumor correlated with the response to neoadjuvant chemotherapy in patients with locally advanced breast cancer. Material and methods: A prospective study of 87 breast cancer patients (Т2-4N0-M0) treated in N.N.Blokhin Russian Cancer Research Center 1997 - 2009. Tumor samples were taken prior to neoadjuvant chemotherapy (cor-biosy). Pathological criteria assessed were: histological variant, tumor grade, HR and Her-2/ neu status, Ki67 expression and glycoprotein Pgp-170 status. After 4-6 cycles of chemotherapy all the patients underwent radical surgery. We quantified the response ix130 | Abstracts Volume 23 | Supplement 9 | September 2012
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Annals of Oncology www.annonc.oxfor
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subscriptions A subscription to Ann
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Annals of Oncology Official Journal
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The European Society for Medical On
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Audit Committee Chair: Fortunato Ci
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Familial cancer Judith Balmaña, Ba
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ESMO 2012 Congress Travel Grants 47
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Exhibitors The following companies
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ESMO Fellowships, 1989-2011 The Eur
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Ondrej Gojis, Czech Republic 2008-2
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abstracts hpv biology and implicati
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abstracts description of intra-tumo
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prevent cell death. It is anticipat
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abstracts a paradigm shift in early
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feasibility), but by how high the c
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mouse model of Kras mutant NSCLC. I
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ESMO-CSCO Joint Symposium: Building
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cytomegalovirus (CMV). Analysis of
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functional consequences of Endoglin
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elationship between the ROR score,
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Disclosure: M. Lee: I am an employe
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plus intravenous Bev(7.5mg/kg q 21d
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anti-EGFR treatment. The present st
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patients harboring a T/T genotype t
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experienced significantly more ≥
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functioning scales. Exploratory ana
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oxaliplatin (100 mg/m 2 )/raltitrex
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minutes. In a previous study, 30-mi
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Conclusions: AMPK and ACC activatio
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of surgical monotherapy in patients
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factors play the determining role i
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were respectively 10.6 vs 8.5 vs 3.
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subgroup. Taking into consideration
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considered sufficient to give an 80
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after Gem-based therapy. The additi
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validate the revised AJCC 7th stagi
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Results: Frequently reported advers
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gastric cancer patients with CNS me
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discriminate the prognosis of HCC p
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prospective, non-interventional stu
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abstracts genitourinary tumors, non
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787O EXTERNAL VALIDATION OF THE ASS
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patient preference for P over S, an
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Hb, PS and LM. Median PFS for patie
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may have led to reduced dose and sh
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Results: 1,622 patients were identi
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RCC) was designed to address an unm
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treatment at week 4, and week 12 by
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Conclusions: In pts with RCC treate
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using Drug inCode ® pharmacogeneti
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efused HDCT. Of 23 patients, 20 com
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Median overall survival (OS) was 26
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abstracts Genitourinary tumors, pro
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and week 13 BPI-SF Q3 scores), 28%
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Working Group (PCWG)-2 guidelines r
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atio HR 0.39; CI 0.18, 0.83, p = 0.
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We observed tumor responses and pro
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Here we report emerging data from t
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945 BONE TURNOVER MARKERS AND POTEN
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952 SEQUENTIAL ANDROGEN DEPRIVATION
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managed in a multidisciplinary (MD)
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or hypercalcemia at screening; prio
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meeting. The prevalence of LGSC is
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physicians in the U.S. and Europe.
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eight patients who had infertility
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same CT/RT; Arm B2: 3 cycles of ind
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patients. We have developed a rando
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anthracyclines in vitro. A favorabl
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than the standard target of ≥2.5
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Patients: From November 2002 to May
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Funding: GSK Biologicals Disclosure
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survival rates of 13-25% (Prieto et
Page 367 and 368:
high response rates and prolonged p
Page 369 and 370:
GlaxoSmithKline, Merck Sharp & Dohm
Page 371 and 372:
advisor for Merck Sharp & Dohme, an
Page 373 and 374:
or cutaneous melanoma. A survival u
Page 375 and 376:
systemic therapy or were intolerant
Page 377 and 378:
abstracts neuroendocrine tumors and
Page 379 and 380:
morbidity, with G3 tumors behaving
Page 381 and 382:
pts. Poorly differentiated endocrin
Page 383 and 384:
Adenocarcinoma was present in 25 pa
Page 385 and 386:
Method: Endobronchial ultrasound gu
Page 387 and 388:
widely used by single agent or plat
Page 389 and 390:
disease after surgery were treated
Page 391 and 392:
stage IIIA NSCLC, EML4-ALK fusion-p
Page 393 and 394:
1200P CONCOMITANT CHEMORADIATION GI
Page 395 and 396:
Patients and methods: The study was
Page 397 and 398:
months (95% CI:13-25). The PFS and
Page 399 and 400:
maintenance therapy had favourable
Page 401 and 402:
abstracts non-small cell lung cance
Page 403 and 404:
Ingelheim, GSK Biologicals (compens
Page 405 and 406:
1234PD RANDOMIZED PHASE III TRIAL O
Page 407 and 408:
GlaxoSmithKline (myself, compensate
Page 409 and 410:
1243P IDENTIFICATION OF MICRORNA (M
Page 411 and 412:
N-arm n=34 P-arm n=32 All n=66 Male
Page 413 and 414:
1255P POPULATION BASED EVALUATION O
Page 415 and 416:
1262P DISTINCT SPREAD OF EGFR MUTAT
Page 417 and 418:
1268P VISUAL DISTURBANCES IN PATIEN
Page 419 and 420:
MERCK SERONO: Advisor, speaker in s
Page 421 and 422:
Conclusions: These data from SAiL a
Page 423 and 424:
NSCLC diagnosis and time of BM diag
Page 425 and 426:
1291P PHASE I/II DOSE-FINDING STUDY
Page 427 and 428:
Network utilization of WBCGF in the
Page 429 and 430:
1303P COST EFFECTIVENESS OF PEMETRE
Page 431 and 432:
Results: The patients’ characteri
Page 433 and 434:
EGFR mut at exons 18, 19, 21, and K
Page 435 and 436:
Methods: EML4-ALK fusion was screen
Page 437 and 438:
Results: The median survival time (
Page 439 and 440:
enefit from sustained EGFR blockade
Page 441 and 442:
epresented by 19 pts (32%) female,
Page 443 and 444:
and at least one prior course of ch
Page 445 and 446:
Methods: NSCLC patients with radiog
Page 447 and 448:
1367TiP LONG-TERM ERLOTINIB THERAPY
Page 449 and 450:
Austria, Czech Republic, Finland, G
Page 451 and 452:
were every 6 weeks (wk) (S1), every
Page 453 and 454:
Advantage enrollees (83% vs. 25%) [
Page 455 and 456:
Results: Based on 10,000 simulation
Page 457 and 458:
cancer tumors 12%, Germ cell tumor
Page 459 and 460:
Material and methods: 50 lung cance
Page 461 and 462:
1414TiP IMPLEMENTATION OF CANCER RE
Page 463 and 464:
abstracts palliative care 1422O EFF
Page 465 and 466:
Method and results: A total of 317
Page 467 and 468:
1436P SURVEY ON MODELS OF INTEGRATI
Page 469 and 470:
care unit (PCU) at the National Can
Page 471 and 472:
Characteristic No. % Total 63 1 st
Page 473 and 474:
hysterectomised-9.10% and cervix ca
Page 475 and 476:
abstracts psycho-oncology 1462PD IN
Page 477 and 478:
events, tumour response, and surviv
Page 479 and 480:
abstracts sarcoma 1477O ADHESION TO
Page 481 and 482:
1481PD A PHASE II STUDY OF DOVITINI
Page 483 and 484:
1488P ORGANISATION OF SARCOMA PATIE
Page 485 and 486:
Patients and methods: From August 2
Page 487 and 488:
chemotherapy respectively. At a med
Page 489 and 490:
of this group Those with relapsed d
Page 491 and 492:
1515 PREDICTORS OF SURVIVAL IN ADOL
Page 493 and 494:
abstracts small cell lung cancer an
Page 495 and 496:
emaining receiving either CAV or to
Page 497 and 498:
1533P EXPRESSION OF WILM⍰TUMOUR G
Page 499 and 500:
more than 3 months after first line
Page 501 and 502:
lower recurrence rate of NE. Pegfil
Page 503 and 504:
egimens (HR = 2.5, p < 0.001). Phys
Page 505 and 506:
1561P PREDICTIVE DIAGNOSTICS FOR RE
Page 507 and 508:
Methods: A prospective multicentre
Page 509 and 510:
Table: 1574P Pharmacokinetic parame
Page 511 and 512:
Novartis and unrestricted research
Page 513 and 514:
studies have shown that chemotherap
Page 515 and 516:
(Grade 1) and moderate to severe (G
Page 517 and 518:
declined to relatively lower level
Page 519 and 520:
1609P PHYSICAL ACTIVITY (PA) AND PH
Page 521 and 522:
patients were admitted to the oncol
Page 523 and 524:
Dicarbamin 100 mg/day on day 5 befo
Page 525 and 526:
Results: Anemia was detected in 83.
Page 527 and 528:
important to carry out randomized s
Page 529 and 530:
abstracts translational research 16
Page 531 and 532:
expression. Then, we analyzed PB sa
Page 533 and 534:
Table: 1657P TH BV + TH HR (95% CI)
Page 535 and 536:
BRAF mutations. Circulating free DN
Page 537 and 538:
1671P PHASE I CLINICAL TRIAL OF CAN
Page 539 and 540:
1678P PREDICTIVE VALUE OF TWO PHENO
Page 541 and 542:
theorized that the PI3K/AKT pathway
Page 543 and 544:
Material and methods: 101 patients
Page 545 and 546:
overexpressing and 232 had triple n
Page 547 and 548:
author index author index A Aamdal
Page 549 and 550:
author index Badran A. ix288 (874)
Page 551 and 552:
author index Bösmüller H. ix209 (
Page 553 and 554:
author index Chen A. ix319 (966O) C
Page 555 and 556:
author index De Droogh E. ix452 (13
Page 557 and 558:
author index Esposito G. ix209 (618
Page 559 and 560:
author index Geiges G. ix306 (930P)
Page 561 and 562:
author index Hartono S. ix70 (155P)
Page 563 and 564:
author index Iwasaki H. ix542 (1694
Page 565 and 566:
author index Kodaira M. ix90 (228P)
Page 567 and 568:
author index Lichtensztejn D. ix350
Page 569 and 570:
author index Martinez A. ix496 (153
Page 571 and 572:
author index Morishita N. ix432 (13
Page 573 and 574:
author index Okamoto N. ix432 (1320
Page 575 and 576:
author index Piau S. ix456 (1401P)
Page 577 and 578:
author index Rodríguez Rodríguez
Page 579 and 580:
author index Scoggins C.R. ix371 (1
Page 581 and 582:
author index Stern L. ix272 (823P)
Page 583 and 584:
author index Trypaki M. ix429 (1308
Page 585 and 586:
author index Whitmore J.B. ix310 (9
Page 587 and 588:
subject index subject index A AAV-H
Page 589 and 590:
subject index ix115 (316TiP), ix116
Page 591 and 592:
subject index diffuse large B-cell
Page 593 and 594:
subject index (1033P), ix340 (1036P
Page 595 and 596:
subject index medical information,
Page 597 and 598:
subject index (612P), ix214 (633),
Page 599 and 600:
subject index RCC, ix274 (830P) re-
Page 601 and 602:
subject index TR-FRET, ix84 (206P)
Page 603 and 604:
drug index drug index 1248P, 1250P,
Page 605 and 606:
translational research index transl
Page 607 and 608:
Page 609:
show all

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